Line
1. The cognitive-perceptual symptoms found in patients with PD include
stress-related state phenomena such as derealization, depersonalization
and illusions, as well as more chronic trait characteristics including
suspiciousness and odd or eccentric thinking. It is important to recall
that similar symptoms may have differing etiologies and severity’s
among diverse PD categories (as well as among Axis I disorders). For
example, referential thinking and paranoid ideation appear related
to a mild thought disorder trait in Cluster A patients but may be
reactive to acute depressive moods among Cluster B patients.
Line
2. Low-dose neuroleptics (NP) are the treatment of first choice for
acute presentations of anger and hostility, suspiciousness, referential
thinking, paranoid ideation, illusions, derealization, and depersonalization.
This recommendation is supported at the highest ("A") level
by randomized, double-blind controlled studies, and open label trials
involving a wide variety of neuroleptics. These studies have been
conducted primarily in borderline and schizotypal patients, in both
inpatient and outpatient settings (Cowdry &: Gardner, 1988; Goldberg
et al., 1986; Soloff, 1986); and in adult and adolescent populations
(Kutcher, Papatheodorou, Reiter, &; Gardner, 1995).
Low-dose
neuroleptics appear to have a broad spectrum of efficacy in acute
use, with effects against symptom severity of depressed mood and impulsively,
as well as against anger-hostility and psychoticism. (Cowdry &;
Gardner, 1988; Soloff et al., 1986b, 1989).
Line
3. Treatment effects appear within days to 2 weeks. Patients with
primary cognitive symptoms respond the best, while patients with a
depressive presentation (and secondary mood-congruent cognitive distortions)
do less well and should be considered for treatments defined for affective
dysregulation.
Line
4. Duration of treatment has been arbitrarily defined by the length
of treatment trials, which are generally 4-6 weeks in acute inpatient
studies and up to 12 weeks in outpatient settings. Prolonged use of
narcoleptic medication in patients with PD has been associated with
progressive noncompliance and dropout. In one continuation study of
BPD subjects treated with haloperidol up to 22 weeks, 87.5% failed
to complete the study, compared to a 58.1% attrition on placebo. Borderline
patients progressively endorsed more depressive complaints and difficulties
with side effects as the duration of the trial proceeded beyond acute
treatment (12 weeks) (Kelly, Soloff, Cornelius, George, & Lis,
1992). An apparent exception to the acute treatment strategy in the
PD patient is a long-term study of depot flupenthixol directed against
the parasuicidal behaviors of patients selected for repeated suicidal
efforts and PD (principally histrionic and borderline) (Montgomery
& Montgomery, 1982). Efficacy against recurrent parasuicidal behaviors
was reported at 4-, 5-, and K-month follow-ups for patients receiving
the depot narcoleptic monthly compared to the injected placebo. Attrition
from this depot trial was low, at 19% overall (22.2% flupenthixol
vs. 15.8% placebo injection). There is currently no research support
for the use of narcoleptic medication as long-term maintenance therapy
in the PD population. The risk of tardive dyskinesia must be weighed
carefully against perceived prophylactic benefit if maintenance strategies
are considered.
Line
5. If response to a low-dose narcoleptic is suboptimal after a "fair
trial'' of 4-6 weeks, the dose should be increased into the ''low''
range suitable for treating Axis I disorders and continued for a second
trial period of 4-6 weeks.
Lines
6, 7, 8. A suboptimal response at this point should prompt re-review
of the etiology of the cognitive-perceptual symptoms. If the symptom
presentation is truly part of a nonaffective syndrome, as in the case
of a Cluster A personality disorder, atypical neuroleptics may be
considered. While there are no double-blind, randomized, placebo-controlled
studies of atypical neuroleptics in the PD population at this time,
open label trials (Frankenburg & Zanarini, 1993) and case studies
(Chengappa, Baker, & Sirri. 1995) have been published supporting
the use of clozapine for patients with BPD and severe, refractory,
psychotic symptoms "of an atypical nature,'' or severe self-mutilation.
In these studies, clozapine was used for patients who had failed previous
neuroleptic trials. Therefore the level of research support for this
decision is "C.'' There is no published literature available
on the treatment of personality disorder patients with risperidol,
olanzapine, or more recent additions to the atypical narcoleptic family
of medications. Line 7. Cognitive-perceptual distortions often present
as mood-congruent symptoms with an affective etiology, although this
is not always apparent on initial evaluation. The need to treat hostility
and paranoid ideation rapidly argues for the use of low-dose neuroleptics
at the start of this algorithm. Where an "affective'' cluster
PD is present, a monoamine oxidase inhibitor (MAOI) or selective serotonin
reuptake inhibitor (SSRI) antidepressant may be added to the low-dose
neuroleptic regimen. This strategy is analogous to the treatment of
Axis I affective disorders with psychotic content, where it is generally
advisable to begin treatment with a neuroleptic before, or at least
concurrently with, an antidepressant. (The use of MAOI and SSRI antidepressants
for affective dysregulation in the PD patient is discussed later.)
In addition to their indication for depressed mood. both MAOI and
SSRI antidepressants have some research support for efficacy against
irritability and anger in the PD patient, findings supported for each
drug class by two or more controlled studies, warranting an "A''
level of support for this recommendation. (Cowdry & Gardner, 1988;
Cornelius, Soloff. Perel, & Ulrich, 1990; Cornelius, Soloff, Perel,
& Ulrich, 1993; Kavoussi, Liu, & Coccaro, 1994; Markovitz,
Calabrese, Schulz, & Meltzer, 19919 Markovitz, 1995; Norden 1989;
Salzman et al., 1995; Soloff et al., 1993).
